The Role of Coagulation and Complement Factors for Mast Cell Activation in the Pathogenesis of Chronic Spontaneous Urticaria.
activated complement factor 5 (C5a)
chronic spontaneous urticaria (CSU)
coagulation factors
complement components
endothelial cells
leukocytes
mast cells
protease activated receptor (PAR)
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
12 07 2021
12 07 2021
Historique:
received:
31
05
2021
revised:
09
07
2021
accepted:
09
07
2021
entrez:
7
8
2021
pubmed:
8
8
2021
medline:
27
10
2021
Statut:
epublish
Résumé
Chronic spontaneous urticaria (CSU) is a common skin disorder characterized by an almost daily recurrence of wheal and flare with itch for more than 6 weeks, in association with the release of stored inflammatory mediators, such as histamine, from skin mast cells and/or peripheral basophils. The involvement of the extrinsic coagulation cascade triggered by tissue factor (TF) and complement factors, such as C3a and C5a, has been implied in the pathogenesis of CSU. However, it has been unclear how the TF-triggered coagulation pathway and complement factors induce the activation of skin mast cells and peripheral basophils in patients with CSU. In this review, we focus on the role of vascular endothelial cells, leukocytes, extrinsic coagulation factors and complement components on TF-induced activation of skin mast cells and peripheral basophils followed by the edema formation clinically recognized as urticaria. These findings suggest that medications targeting activated coagulation factors and/or complement components may represent new and effective treatments for patients with severe and refractory CSU.
Identifiants
pubmed: 34359930
pii: cells10071759
doi: 10.3390/cells10071759
pmc: PMC8306267
pii:
doi:
Substances chimiques
Receptors, Proteinase-Activated
0
Complement System Proteins
9007-36-7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
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